KYJ7-MAP- Mean Arterial Pressure
Knowing your Jargon (KYJ)
In this episode of KYJ we explore the forgotten vital sign. Mean arterial pressure. Indirectly we obtain it from the patient's BP.
The MAP is what I call the Magic number. It is a determination of the net flow of blood perfusing organs. Measured as a pressure it is calculated by adding the diastolic BP to one third of the pulse pressure. Confused???
Look its easy- start with an example- BP is 110/70
Pulse pressure = systolic - Diastolic.
Do this bit first : 110-60 =50
Pulse pressure is 50.
Now take 1 third of this PP
50 / 3 = 16.66 (round up to 17)
Now add this 17 to the Diastolic (60)
17+60
MAP= 77. See, so simple.
Now the mean pressure of blood going through brain , heart, lungs, kidneys and all other organs is a direct result of the MAP.
The MAP in an adult should be between 70-110.
Above 110 (hypertension), physical damage to vessels in the kidneys,eyes and brain may occur. Stroke risk is high.
So at what point is MAP considered to be too low to offer adequate perfusion . 55-60 is our critical point where kidney perfusion suffers. So aiming for a Magic number of 60 is desirable.
Below 55 brain and cardiac function starts to deteriorate.
Next time you use an electronic BP machine, look carefully at the display- most machines calculate that MAP for You.
It's a Magic number!!
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Thursday, 26 December 2013
6- IE Ratio
KYJ6 - IE ratio
Knowing your Jargon.
In this episode of KYJ (Knowing your Jargon, not to be confused with KY Jelly), we look at one of the forgotten respiratory assessment data. The humble IE ratio is often observed, yet rarely recorded. It stands for Inspiratory :Expiratory. It is a ratio of time that it takes for a person to inhale a breath, vs the time it takes to exhale.
Normally we take 1.5 to twice as long to breathe out than we do to breathe in. Therefore our normal IE Ratio is expressed as between 1:1.5 to 1:2 .
This simply means if it took you one second to breathe in, it would be normally expected that you'd take 1.5 - 2 secs to breathe out. This becomes a function of lung compliance and air way obstruction.
Lets consider two extremes .
Scenario 1 a high IE ratio of 3:1
In this example, a person takes 3 times longer to inhale than exhale. In upper respiratory stridor eg croup, or foreign body airway obstructions, the difficulty might be getting a lung full in. We see this in circumferential chest burns also; and if severe enough, a surgical skin release procedure called Escarotomy, is performed to release pressure.
Scenario 2
In Low IE ratios, the patient has no trouble breathing in, but may exhibit difficulty exhaling due to lower airways restriction, or bronchospasm. A classic example is the acute Asthma patient who may have breathing so laboured, that an IE ratio is something like 1:5. It takes 5 times longer to exhale that inhale. In children with restrictive airways diseases like asthma, the lower the IE ratio, the more exhausted they get. Gas trapping occurs followed by respiratory failure and arrest.
... Just a KYJ quicky tonight.
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5-high VQ= dead space
KYJ5 - Dead space.
Knowing you Jargon
Previously, we covered VQ mismatch with low VQ otherwise called "shunt".
This episode we look at its opposite. High VQ is called dead space.
Dead space refers to a disproportionately high volume of air to blood ratio in the lungs.
In respiratory presentations where a lung can ventilate or fill with air, but a vascular obstruction has occurred, the air doesn't have an opportunity to
Give up oxygen or diffuse CO2.
Such a condition is seen in a pulmonary embolism (PE). Due to a blood clot obstructing a segment of pulmonary vessels, blood can't flow through lobules or segments of lung. Air in these sections ventilate well enough, but with no blood flow, there is no diffusion. These patients are said to
Have a high VQ or dead space.
VQ is usually 4l air : 5 l blood
Making a VQ ratio of 0.8.
If I reduce (block) blood flow I might see a High VQ of 4l air :3l blood or a VQ = 1.33
...
Less blood perfusing lung = lower oxygen in blood (Hypoxaemia) and high CO2 ( hypercapnoea).
This leads first to a Respiratory acidosis then a mixed metabolic acidosis as hypoxic cells start enter anaerobic metabolism and produce Lactic Acid.
Treatment of High VQ or Dead space is to, oxygenate optimally, and restore blood flow.
Empirically, anticoagulants were used, typically Heparin. Prior to
This regimen, 30% of PE patients died, but with anti coagulation the mortality is less than 9%.
Improvements currently available include thrombolysis. Where a plasminogen activator is administered to encourage the patients own enzyme system to seek and dissolve the fibrin clot.
Improvements in testing and diagnosis also reduces ischaemia time, which is the ultimate goal.
...
If you enjoyed this snipet. Please share on your page and with your friends.
Knowing you Jargon
Previously, we covered VQ mismatch with low VQ otherwise called "shunt".
This episode we look at its opposite. High VQ is called dead space.
Dead space refers to a disproportionately high volume of air to blood ratio in the lungs.
In respiratory presentations where a lung can ventilate or fill with air, but a vascular obstruction has occurred, the air doesn't have an opportunity to
Give up oxygen or diffuse CO2.
Such a condition is seen in a pulmonary embolism (PE). Due to a blood clot obstructing a segment of pulmonary vessels, blood can't flow through lobules or segments of lung. Air in these sections ventilate well enough, but with no blood flow, there is no diffusion. These patients are said to
Have a high VQ or dead space.
VQ is usually 4l air : 5 l blood
Making a VQ ratio of 0.8.
If I reduce (block) blood flow I might see a High VQ of 4l air :3l blood or a VQ = 1.33
...
Less blood perfusing lung = lower oxygen in blood (Hypoxaemia) and high CO2 ( hypercapnoea).
This leads first to a Respiratory acidosis then a mixed metabolic acidosis as hypoxic cells start enter anaerobic metabolism and produce Lactic Acid.
Treatment of High VQ or Dead space is to, oxygenate optimally, and restore blood flow.
Empirically, anticoagulants were used, typically Heparin. Prior to
This regimen, 30% of PE patients died, but with anti coagulation the mortality is less than 9%.
Improvements currently available include thrombolysis. Where a plasminogen activator is administered to encourage the patients own enzyme system to seek and dissolve the fibrin clot.
Improvements in testing and diagnosis also reduces ischaemia time, which is the ultimate goal.
...
If you enjoyed this snipet. Please share on your page and with your friends.
4- low VQ =shunt
KYJ-4 Respiratory Shunt
What is a Shunt?
Often nurses hear that the patient has a VQ mismatch or Shunt, with respect to respiratory nursing.
"V" – ventilation – the air that reaches the alveoli
"Q" – perfusion – the blood that reaches the alveoli
These two variables constitute the main determinants of the blood oxygen concentration.
Given that our ventilation to perfusion ratio is approximately 4 litres of air, coming into contact with about 5 litres of blood, our VQ (ventilation/perfusion) is mathematically calculated as 4/5 or 0.8.
In a situation that our VQ is very low, where more blood goes through the lungs than usually contacts air , it is referred to as a Shunt. Think blood shunting through lungs but not being able to gas exchange.
Classic examples are foreign body airway obstructions, pulmonary oedema, pneumonia and restrictive airways diseases like asthma.
Blood continues to circulate (shunt) through the pulmonary vasculature but with limited air, gas exchange is adversely affected. The patient is classically hypoxaemic (low Spo2) and potentially acid optic due to inability to blow off building CO2.
Shunt = low VQ ratio.
More blood, less air.
...
If you have a jargon term you want to get your head around, let us know and I'll feature it in an upcoming episode of "know your jargon".
What is a Shunt?
Often nurses hear that the patient has a VQ mismatch or Shunt, with respect to respiratory nursing.
"V" – ventilation – the air that reaches the alveoli
"Q" – perfusion – the blood that reaches the alveoli
These two variables constitute the main determinants of the blood oxygen concentration.
Given that our ventilation to perfusion ratio is approximately 4 litres of air, coming into contact with about 5 litres of blood, our VQ (ventilation/perfusion) is mathematically calculated as 4/5 or 0.8.
In a situation that our VQ is very low, where more blood goes through the lungs than usually contacts air , it is referred to as a Shunt. Think blood shunting through lungs but not being able to gas exchange.
Classic examples are foreign body airway obstructions, pulmonary oedema, pneumonia and restrictive airways diseases like asthma.
Blood continues to circulate (shunt) through the pulmonary vasculature but with limited air, gas exchange is adversely affected. The patient is classically hypoxaemic (low Spo2) and potentially acid optic due to inability to blow off building CO2.
Shunt = low VQ ratio.
More blood, less air.
...
If you have a jargon term you want to get your head around, let us know and I'll feature it in an upcoming episode of "know your jargon".
3- INR and APTT
KYJ3 - INR and APTT .
Knowing your Jargon- What is the difference?
Patients on Warfarin are often monitored with regular blood tests called International Normalised Ratio or INR for short.
Heparinised patients will have a blood test called Activated Partial Thromboplastin Time (APTT).
To understand the two tests you first need to understand how both the anticoagulants work
Heparin and Warfarin work differently.
Heparin destroys thrombin indirectly by stimulating an enzyme AT3.
Warfarin inhibits the precursor to Thrombin. A protein called Prothrombin.
So when measuring Prothrombin Time (PT) the INR looks at how long prothrombin takes to convert into Thrombin.
If prothrombin is inhibited by warfarin, the prothrombin time is delayed.
With APTT, this test looks at the time it takes for Thromboplastin (sticky gooyness of plasma) to form once the test sample has been activated.
Nerdy topic, but I know you were wondering!
Knowing your Jargon- What is the difference?
Patients on Warfarin are often monitored with regular blood tests called International Normalised Ratio or INR for short.
Heparinised patients will have a blood test called Activated Partial Thromboplastin Time (APTT).
To understand the two tests you first need to understand how both the anticoagulants work
Heparin and Warfarin work differently.
Heparin destroys thrombin indirectly by stimulating an enzyme AT3.
Warfarin inhibits the precursor to Thrombin. A protein called Prothrombin.
So when measuring Prothrombin Time (PT) the INR looks at how long prothrombin takes to convert into Thrombin.
If prothrombin is inhibited by warfarin, the prothrombin time is delayed.
With APTT, this test looks at the time it takes for Thromboplastin (sticky gooyness of plasma) to form once the test sample has been activated.
Nerdy topic, but I know you were wondering!
C Collar- trauma pearl #3
Trauma pearls #3
When does the collar get applied?
You've done the courses, or heard the rhetoric, Airway with simultaneous C-spine stabilisation, breathing, circulation, disability.
The doctrine , dogma, cornerstone of trauma patient assessment. But what of the collar? When does it actually get applied? For years there has been a teaching of its importance, but exactly in the primary and secondary assessment sequence is it most appropriate to apply?
The historical notion of Airway and simultaneous C-spine precautions stemmed from the old inappropriate resuscitation practice of checking airway by rolling the patient to the side and tilting (hyper extending ) the patient's head. In a trauma patient this manoeuvre would potentially harm a high spinal injured patients spinal cord. Thus the techniques of chin lift and jaw thrust were developed to open airways without tilting the head. The full stabilisation and immobilisation of the spine, including the application of spinal C-collar , back board and head blocks came later, but somehow got confused in the sequencing.
Don't put the collar on in A!
Back to the intent of Airway assessment, we see it is about "do no harm". Hold that neck still while you are assessing and managing that airway. It was never about applying a collar. Manual inline stabilisation means using a colleague to hold the head still.
Now think about this; you don't want me wasting time sizing, and applying a c-collar, when I have not even assessed if you are breathing, or have a heart beat do you? No. These are far to important to delay. So put off collar fitting till later.
When?
Well the C collar is just another gadget so after "E" exposing the patient, go for it. Or even apply as the last thing before the log roll, but don't delay your Primary assessment. Nothing is gained by application of a collar.
When does the collar get applied?
You've done the courses, or heard the rhetoric, Airway with simultaneous C-spine stabilisation, breathing, circulation, disability.
The doctrine , dogma, cornerstone of trauma patient assessment. But what of the collar? When does it actually get applied? For years there has been a teaching of its importance, but exactly in the primary and secondary assessment sequence is it most appropriate to apply?
The historical notion of Airway and simultaneous C-spine precautions stemmed from the old inappropriate resuscitation practice of checking airway by rolling the patient to the side and tilting (hyper extending ) the patient's head. In a trauma patient this manoeuvre would potentially harm a high spinal injured patients spinal cord. Thus the techniques of chin lift and jaw thrust were developed to open airways without tilting the head. The full stabilisation and immobilisation of the spine, including the application of spinal C-collar , back board and head blocks came later, but somehow got confused in the sequencing.
Don't put the collar on in A!
Back to the intent of Airway assessment, we see it is about "do no harm". Hold that neck still while you are assessing and managing that airway. It was never about applying a collar. Manual inline stabilisation means using a colleague to hold the head still.
Now think about this; you don't want me wasting time sizing, and applying a c-collar, when I have not even assessed if you are breathing, or have a heart beat do you? No. These are far to important to delay. So put off collar fitting till later.
When?
Well the C collar is just another gadget so after "E" exposing the patient, go for it. Or even apply as the last thing before the log roll, but don't delay your Primary assessment. Nothing is gained by application of a collar.
Platelets
Getting to know the Platelets .
These are funky little dudes. The are about a third of the size of a red blood cell meaning they can fit through the narrowest of places.
Platelets are dynamic living cell particles with no nucleus. So they can't reproduce. Specialised bone marrow cells called Megakaryocytes make the platelets by breaking in to fragments called Thrombocytes or platelets.
They live for about 7-10 days.
The role of platelets is twofold
First they form a thrombus or clot by aggregating (just a fancy word for "group hug"
But how is this group hug initiated?
Glad you asked. After being activated by contact with tissue collagen or the exposed damaged blood vessel wall, platelets send out signalling chemicals (cytokines) to other platelets to come join the party. One such cytokines is Thromboxane A2 (TXA2)
Think of TXA2 as a message on the platelet's facebook page ... Saying "party, my place, bring your mates!!"
One platelet sticks to another with two glues. VonWillebrand factor and Fibrinogen. These plasma proteins allow clumping of the mass of platelets to form a primary clot.
Another Glycoprotein which I call "Gloop" sticks the clot to the wall of the vessel. If it fails, the clot mobilises and is called an Embolism.
Meanwhile, these chemical cocktails being released from activated platelets initiate the whole coagulation cascade which ultimately converts that sticky fibrinogen in to strands of fibrin. Think of fibrin as a fishnet knitting the platelets together to stabilise them.
Deep inside the platelet are proteins of Actin and Myocin which contract together to cause the bundle of platelets to squeeze tight.
The who thing is just so clever.
Aspirin inhibits the release of that signalling protein TXA2. Making aspirin an important drug in the Acute Coronary Syndrome patient.
An alternative anti platelet drug is Clopidogrel (Plavix). This drug defeated and permanently disarms the P2Y receptor on the platelet surface. These sites are the bits of the platelet that attaches other platelets when they are having that group hug.
These are funky little dudes. The are about a third of the size of a red blood cell meaning they can fit through the narrowest of places.
Platelets are dynamic living cell particles with no nucleus. So they can't reproduce. Specialised bone marrow cells called Megakaryocytes make the platelets by breaking in to fragments called Thrombocytes or platelets.
They live for about 7-10 days.
The role of platelets is twofold
First they form a thrombus or clot by aggregating (just a fancy word for "group hug"
But how is this group hug initiated?
Glad you asked. After being activated by contact with tissue collagen or the exposed damaged blood vessel wall, platelets send out signalling chemicals (cytokines) to other platelets to come join the party. One such cytokines is Thromboxane A2 (TXA2)
Think of TXA2 as a message on the platelet's facebook page ... Saying "party, my place, bring your mates!!"
One platelet sticks to another with two glues. VonWillebrand factor and Fibrinogen. These plasma proteins allow clumping of the mass of platelets to form a primary clot.
Another Glycoprotein which I call "Gloop" sticks the clot to the wall of the vessel. If it fails, the clot mobilises and is called an Embolism.
Meanwhile, these chemical cocktails being released from activated platelets initiate the whole coagulation cascade which ultimately converts that sticky fibrinogen in to strands of fibrin. Think of fibrin as a fishnet knitting the platelets together to stabilise them.
Deep inside the platelet are proteins of Actin and Myocin which contract together to cause the bundle of platelets to squeeze tight.
The who thing is just so clever.
Aspirin inhibits the release of that signalling protein TXA2. Making aspirin an important drug in the Acute Coronary Syndrome patient.
An alternative anti platelet drug is Clopidogrel (Plavix). This drug defeated and permanently disarms the P2Y receptor on the platelet surface. These sites are the bits of the platelet that attaches other platelets when they are having that group hug.
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